p53Arg72Pro polymorphism of tumour suppressor protein is associated with luminal narrowing after coronary stent placement.

T he cause of in-stent luminal narrowing has been primarily considered to be neointimal hyperplasia that is caused by proliferating vascular smooth muscle cells (VSMC). It has been recently reported that local drug delivery systems produce good results for the inhibition of VSMC proliferation. The potential of suppressive agents in the treatment of in-stent luminal narrowing arises from basic studies according to cell cycle regulation and gene expression. p53 is a tumour suppressor protein involved in regulating the growth of VSMC. Loss of p53 activity results in the growth of VSMC, while increased concentrations of p53 result in apoptosis of VSMC. A common polymorphism in the p53 amino acid sequence which results in the presence of either arginine (Arg) or proline (Pro) at position 72 may influence the susceptibility to malignancy through its interaction with p73. The effects of this polymorphism on p53 function seem to be related to p73, and p53Arg was reported to be more susceptible to the inactivation of p73 than p53Pro alleles. It is conceivable that this common polymorphism of p53, Arg72Pro, may also influence VSMC proliferation after coronary stent implantation. In the present study, we tested this hypothesis in patients after coronary stent implantation using quantitative coronary angiography.